Roles of TRAF5 in the lineage commitment of helper T cell subsets

2014 Fiscal Year Final Research Report

• Project/Area Number: 24590571
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: Tohoku University
• Principal Investigator: SO Takanori 東北大学, 医学(系)研究科(研究院), 准教授 (60294964)
• Co-Investigator(Kenkyū-buntansha): ISHII Naoto 東北大学, 医学系研究科, 教授 (60291267)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: ヘルパーT細胞 / CD4+ T細胞 / TRAF5 / Th17 / シグナル伝達 / 自己免疫 / サイトカイン / TRAF

Outline of Final Research Achievements

Helper T-lymphocytes (Th cells) promotes immune-mediated inflammatory diseases, such as allergic asthma and rheumatoid arthritis. Signaling via IL-6 contributes to the development of the Th17 subset, which is one of major subpopulations of Th cells. Th17 cells activate neutrophils and are involved in autoimmune diseases. This study demonstrates that TRAF5 adaptor protein constitutively associates with a cytoplasmic region in the signaling transducing receptor for IL-6, gp130, to inhibit the IL-6 signaling and that TRAF5 works as an anti-inflammatory factor to limit immune responses mediated by pathogenic Th17 cells.

Free Research Field

免疫学